Superdrol

Methasterone (also marketed as Superdrol) is a synthetic anabolic-androgenic steroid belonging to the dihydrotestosterone (DHT) derivative class. Chemically, it is 2α,17α-dimethyl-5α-androstan-17β-ol-3-one, meaning it carries methyl groups at both the 2α and 17α positions of the androstane skeleton. The 17α-methyl substitution is the structural feature most associated with oral bioavailability, as it resists first-pass hepatic metabolism that would otherwise rapidly inactivate the molecule.

Because methasterone lacks the Δ4-3-keto arrangement typical of aromatizable steroids, it does not convert to estrogen via aromatase. It binds the androgen receptor and exerts potent androgenic and anabolic activity in tissues. The compound has appeared as an undeclared ingredient in over-the-counter dietary supplements and has been classified as a Schedule III controlled substance in the United States.

Animal study: In humanized (uPA+/+-SCID chimeric) mice transplanted with human hepatocytes, a single administration of methasterone (Superdrol) resulted in urinary excretion of several metabolites including a 3-keto reduced metabolite and multiple hydroxylated metabolites, characterizing its phase I and phase II metabolic profile. Note: Doping/detection study; humanized mouse model used (PMID 21762781)

Laboratory study: Luciferase reporter assays demonstrated that methasterone and extracts of implicated supplement capsules were highly androgenic via androgen receptor activation, and this androgenicity persisted for several days after cell exposure. (PMID 36796473)

Laboratory study: In a cell-based nitric oxide inhibition assay, methasterone itself showed significant anti-inflammatory activity, and microbial biotransformation with Glomerella fusarioides produced derivatives with varying degrees of NO inhibitory activity, while all new derivatives were non-cytotoxic to human fibroblast cells. Note: Microbial biotransformation study (PMID 36893829)

Laboratory study: Microbial transformation of methasterone with two fungi produced six structural derivatives, and methasterone itself showed anti-inflammatory activity comparable to a standard inhibitor in a nitric oxide production assay, though the parent compound was cytotoxic to a normal human cell line while its metabolites were not. Note: Microbial biotransformation study (PMID 35424863)

Laboratory study: Biotransformation of methasterone with three fungal species produced thirteen metabolites, one of which showed potent inhibition of the pro-inflammatory cytokine TNF-α far exceeding the standard reference compound, suggesting methasterone derivatives may have immunomodulatory properties. Note: Microbial biotransformation study (PMID 28404456)

Laboratory study: A spectroscopic and computational study found that methasterone binds bovine serum albumin spontaneously through hydrogen bonding and van der Waals forces, forming a stable ground-state complex that slightly alters protein conformation, providing foundational data on its protein-binding behavior. (PMID 39983858)

Laboratory study: In vitro stability testing showed that dimethazine degrades to methasterone, and human liver microsome and chimeric mouse studies confirmed that methasterone metabolites account for all major metabolites of dimethazine, indicating that screening for methasterone is sufficient for detecting dimethazine misuse. Note: Doping/detection study; dimethazine (azine dimer of methasterone) studied (PMID 26663462)

Human study: Chemical analysis of vitamin and multimineral supplements implicated in an outbreak among approximately 16 New York residents detected methasterone, dimethazine, and methylstenbolone as undeclared ingredients; adverse effects in exposed individuals included fatigue, hair loss, muscle aches, liver damage requiring hospitalization, and severe virilization in a child. Note: Found as undeclared ingredient in OTC dietary supplements (PMID 36796473)

Human study: A case report described a patient who developed cholestatic jaundice and IgA nephropathy after using an OTC muscle-building supplement containing methasterone (Superdrol), with IgA nephropathy being a previously unreported association with androgenic steroid use. Note: OTC supplement sold as Superdrol (PMID 16952289)

Human study: A case report documented a young man who developed transient cholestatic hepatitis followed by severe hepatitis-associated aplastic anemia after using the anabolic steroid methasterone, representing a rare and serious hematologic complication. (PMID 25314890)

Laboratory study: An in vitro and computational study found that methasterone inhibits the hepatic enzyme AKR1D1, which is involved in bile acid synthesis, suggesting a potential mechanism by which methasterone could contribute to hepatotoxicity through disruption of bile acid metabolism. (PMID 37451653)

Limitations:

Human study: The in vivo metabolic study enrolled only a very small number of healthy volunteers, limiting generalizability of the metabolic profile and detection window findings to broader populations. Note: Doping/detection study (PMID 39883123)

Open questions: Several important questions remain unanswered by current evidence. Almost all human metabolic data come from single-volunteer administration studies, making it impossible to know how biological variability, body composition, or co-ingested substances affect the metabolic profile or detection window. The precise mechanism by which methasterone triggers cholestatic liver injury and rare sequelae such as aplastic anemia is not established, nor is it known whether these events are dose-dependent or idiosyncratic. The compound's inhibition of AKR1D1 has only been demonstrated in vitro, so the clinical relevance of this pathway to observed hepatotoxicity in people has not been confirmed.

The anti-inflammatory activity observed in cell-based and microbial-transformation studies has not been tested in any animal model or human trial. Long-term androgenic and cardiovascular effects specific to methasterone, distinct from other anabolic steroids, have not been studied systematically.